Propofol directly depresses lumbar dorsal horn neuronal responses to noxious stimulation in goats

Antognini, Joseph F.; Wang, Xiao Wei; Piercy, Marla; Carstens, Earl

doi:10.1007/bf03018926

Cited by 54 publications

(40 citation statements)

References 26 publications

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“…It was found that the analgesic effect of propofol may result as it potentiate the functions of GABAA receptors [20]. Our results were in agreement with Antognini et al [21] who found propofol directly repress the lumbar dorsal horn neuronal responses to noxious stimulation when goats were infused with propofol intravenously. However, Jugovac [13] found that propofol could not decrease the TPR score Intracerebroventricularly, indicating that propofol has no analgesia effect.…”

Section: Discussionsupporting

confidence: 93%

Connection Changes in Somatosensory Cortex Induced by Different Doses of Propofol

Liu

Zhang

et al. 2014

PLoS ONE

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BackgroundThe mechanism by which general anesthetics, widely used in clinical practice for over 160 years, effects on sensory responsiveness has been unclear until now. In the present study, the authors sought to explore the effect of different doses of propofol on somatosensory cortex by whisker stimulation in rats.MethodsIn a fixed cage, rats were anesthetized with propofol 80 mg/kg intraperitoneally and then cathetered tail vein with 23-gauge metal needle connected with a pump. Two holes (2 mm diameter) were drilled and recording electrodes implantated in the primary somatosensory cortex barrel field (S1BF) and secondary somatosensory cortex (S2). The extracellular (20 rats) and intracellular (8 rats) recordings were used to test the neuron activity in both cortices at different doses of propofol (20, 40 and 80 mg/kg/h) through tail vein by pump. Meantime, vibrissal, olfactory, corneal responses (VOCR, sedation), and tail-pinch response (TRP, analgesia) were tested every 10 min during the doses of propofol 20, 40 and 80 mg/kg/h.ResultsVOCR and TRP were depressed by propofol in a dose-dependent manner. The amplitude by whisker stimulation in S1BF was stronger and the peak latency was shorter compared with that of in S2. The response latency of S1BF and S2 was increased by raising infusion rate of propofol with the response latency in S2 being longer than that in S1BF at the same doses of propofol. The cross-correlation between S1BF and S2 decreased as the propofol infusion rate increased. The input resistance was higher by increasing infusion rate of propofol.ConclusionThe sedation and analgesia effects of propofol were dose-dependent. Both the connectivity and instinctive oscillation between S1BF and S2 were proportionally modulated by the different doses of propofol.

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Section: Discussionsupporting

confidence: 93%

Connection Changes in Somatosensory Cortex Induced by Different Doses of Propofol

Liu

Zhang

et al. 2014

PLoS ONE

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“…12, 13 We had hypothesized that the depressant effects of an anesthetic such as propofol, which acts primarily via GABA A receptors, 8 may depress neurons with ascending projections to a greater degree, as suggested by Soja et al's 3 work in cats. In our study the depressant effects of propofol on response to noxious heat were similar in neurons with and without identifiable ascending projections to the cervical cord, similar to the findings of Paik et al 4 who reported no difference in the depressant effect of sodium pentobarbital on cat dorsal horn neurons, regardless of whether they could be antidromically activated from the thoracic spinal cord.…”

Section: Discussionmentioning

confidence: 97%

Immobilizing Doses of Halothane, Isoflurane or Propofol, Do Not Preferentially Depress Noxious Heat-Evoked Responses of Rat Lumbar Dorsal Horn Neurons with Ascending Projections

Barter

Mark

Jinks

et al. 2008

Anesthesia &Amp; Analgesia

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BACKGROUND-The spinal cord is an important site where volatile anesthetics decrease sensation and produce immobility. Beyond this knowledge, our understanding of a site of anesthetic action is limited. Previous evidence suggests that dorsal horn neurons with ascending projections may be more susceptible to depression by general anesthetics than local spinal interneurons. In this study we evaluated the effects of volatile and injectable general anesthetics on lumbar dorsal horn neurons with and without ascending projections.

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“…Previous studies have shown significant depression of the dorsal horn by propofol and isoflurane, 8–11 leading to the hypothesis that immobility could be the result of depression at the dorsal horn. In addition, anesthetics depress neurons in the ventral spinal cord, which includes motoneurons and central pattern generators, with the latter group of neurons being particularly sensitive to anesthetics.…”

mentioning

confidence: 99%

Propofol Produces Immobility via Action in the Ventral Horn of the Spinal Cord by a GABAergic Mechanism

Kungys¹,

Kim²,

Jinks³

et al. 2009

Anesthesia &Amp; Analgesia

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Background We investigated the actions of propofol and isoflurane on nociceptive responses of neurons in the spinal cord. Methods We determined nociceptive responses of lumbar neurons in the dorsal horn (<1200 μm) and ventral horn (>1200 μm) of decerebrate rats before and during propofol (1 effective dose, ED50) or isoflurane (1 minimum alveolar concentration) anesthesia. During recording of ventral horn neurons, we administered picrotoxin by infusion to determine whether isoflurane and propofol differed in their effects at the gamma amminobutyric acid (GABA) Type A receptors. We also determined whether decerebration altered propofol requirements to produce immobility. Results Decerebration did not affect propofol requirements. The ED50 for propofol was 497 ± 58 μg/kg/min in intact rats and 420 ± 65 μg/kg/min in decerebrated rats (p>0.05), with corresponding propofol blood concentrations of 8.1 ± 1.1 μg/ml and 7.3 ± 1.1 μg/ml, respectively (p>0.05). Propofol did not significantly depress dorsal horn neurons, but isoflurane depressed the responses to 56% of control (p<0.05). Propofol depressed ventral horn neurons to 47% of control, whereas isoflurane depressed ventral horn neurons to 20% of control. Picrotoxin significantly reversed the depressant effect of propofol on ventral horn neuronal responses (79% of control, not significantly different from control). Picrotoxin, however, had no effect on isoflurane’s depression of ventral horn neuronal responses (26% of control). Conclusions Propofol acts in the spinal cord to produce immobility. This depressive effect occurs in the ventral horn and is mediated mainly by GABAA receptors. Isoflurane also depresses neurons in the ventral horn; however, isoflurane actions at the GABAA receptor are either weak or overridden by other effects in the ventral horn.

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Propofol directly depresses lumbar dorsal horn neuronal responses to noxious stimulation in goats

Abstract: These data indicate that propofol has a direct depressant effect on dorsal horn neuronal responses to noxious stimulation, with little or no indirect supraspinal effect.

Cited by 54 publications

References 26 publications

Connection Changes in Somatosensory Cortex Induced by Different Doses of Propofol

Connection Changes in Somatosensory Cortex Induced by Different Doses of Propofol

Immobilizing Doses of Halothane, Isoflurane or Propofol, Do Not Preferentially Depress Noxious Heat-Evoked Responses of Rat Lumbar Dorsal Horn Neurons with Ascending Projections

Propofol Produces Immobility via Action in the Ventral Horn of the Spinal Cord by a GABAergic Mechanism

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